Cross talk between cell death and cell cycle progression: BCL-2 regulates NFAT-mediated activation

Gerald P. Linette; Ying Li; Kevin Roth

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Cross talk between cell death and cell cycle progression: BCL-2 regulates NFAT-mediated activation

机译：细胞死亡与细胞周期进程之间的串扰：BCL-2调节NFAT介导的激活

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BCL-2-deficient T cells demonstrate accel- erated cell cycle progression and increased apoptosis follow- ing activation. Increasing the levels of BCL-2 retarded the G_0 S transition, sustained the levels of cyclin-dependent kinase inhibitor p27~Kip1, and repressed postactivation death. Proximal signal transduction events and immediate early gene transcription were unaffected.

机译：缺乏BCL-2的T细胞表现出加速的细胞周期进程和激活后凋亡增加。 BCL-2的水平升高会延缓G_0 S的转换，维持细胞周期蛋白依赖性激酶抑制剂p27〜Kip1的水平，并抑制激活后死亡。近端信号转导事件和立即早期基因转录不受影响。

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《Proceedings of the National Academy of Sciences of the United States of America》 |1996年第18期|p.9545-9552|共8页
作者
Gerald P. Linette; Ying Li; Kevin Roth;
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收录信息美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
原文格式 PDF
正文语种 eng
中图分类自然科学总论;
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6. Cross talk between cell death and cell cycle progression: BCL-2 regulates NFAT-mediated activation. [O] . G P Linette, Y Li, K Roth, 1996

机译：细胞死亡与细胞周期进程之间的相互影响：BCL-2调节NFAT介导的激活。
7. Cross talk between cell death and cell cycle progression: BCL-2 regulates NFAT-mediated activation. [O] . Linette, G P, Li, Y, Roth, K, 1996

机译：细胞死亡与细胞周期进程之间的相互影响：BCL-2调节NFAT介导的激活。

Cross talk between cell death and cell cycle progression: BCL-2 regulates NFAT-mediated activation

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